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ALS > Block 3 > Flashcards

Block 3 Flashcards

1
Q

what are the three phases of swallowing?

A
  1. oral phase
  2. pharyngeal phase
  3. oesophageal phase
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2
Q

what happens at the oral phase? (2)

A
  • voluntary phase
  • tongue pushing bolus to the back of the throat
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3
Q

what happens at the pharyngeal phase? (5)

A
  • tongue blocks oral cavity
  • soft palate blocks nasal cavity
  • vocal folds close to protect airways
  • oesophageal sphincter opens
  • stimulated by tactile receptors in the oropharynx
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4
Q

what happens at the oesophageal phase? (3)

A
  • bolus propelled down oesophagus by peristalsis
  • larynx moves back to original position
  • peristaltic waves moves gastric contents down into pyloric antrum
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5
Q

what nerve innervates the muscles of mastication?

A

trigeminal nerve

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6
Q

what is the chewing reflex controlled by?

A

nuclei in the brainstem

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7
Q

stages of the chewing reflex (5)

A
  • presence of bolus initiates reflex inhibition of muscles, allows jaw to drop
  • drop initiates stretch reflex of jaw muscles
  • leads to rebound contraction, automatically raising jaw to cause closure of teeth
  • compression of bolus against the lining of the mouth inhibits the jaw muscles again
  • process is repeated
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8
Q

What is retropulsion?

A

food particles that are too large to pass through the pyloric sphincter into the small intestine are forced back into the body of the stomach

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9
Q

three phases of gastric acid secretion

A
  1. cephalic phase - secretion by anticipation of eating (smell/taste)
  2. gastric phase - secretion stimulated by distension of the stomach and by amino acids present in the food
  3. intestinal phase - stimulated by small intestine digestion and by amino acids
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10
Q

What are the stages of the secretion of gastric acid (5)

A
  • Cl- and Na+ are secreted actively from parietal cells into the lumen of the canaliculus
  • this creates a negative potential across the membrane that causes K+ and some Na+ to diffuse out
  • carbonic anhydrase catalyses the reaction between CO2 and H2O to form carbonic acid. This dissociates into H+ and HCO3-
  • H+ leave the cell through H+K+ ATPase anti porter, at the same time Na+ is actively reabsorbed
  • H+ and Cl- mix together, they are secreted into the lumen the oxyntic gland
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11
Q

What is gastric emptying?

A

when the food particles are small enough they can pass through the pyloric sphincter

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12
Q

What does the cephalic phase of gastric activate? (3)

A
  • cerebral cortex
  • hypothalamus
  • brain stem
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13
Q

what two components make up chyme?

A
  • food particles
  • gastric acid
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14
Q

Which nerves activate the stimulation of the salivary glands? (2)

A
  • facial nerve
  • glossopharyngeal nerve
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15
Q

What is released through the stimulation of gastric glands?

A

gastric jucie

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16
Q

which nerve activates the stimulation of the gastric glands?

A

vagus nerve

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17
Q

which cells release gastrin?

A

G cells

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18
Q

What is gastrin released in response to? (5)

A
  • distention
  • high pH
  • caffeine
  • Ach
  • partially digested proteins
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19
Q

What does gastrin do? (4)

A
  • increase motility of stomach
  • relaxed pyloric sphincter
  • strengthens contraction of lower oesophageal sphincter to prevent reflux
  • stimulates gastric glands to secrete large amounts of gastric juice
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20
Q

What pH is gastrin secretion inhibited at?

A

pH <2

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21
Q

What is absorbed in the duodenum?

A

iron

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22
Q

What is absorbed in the jejunum? (4)

A
  • folate
  • glucose
  • fatty acids
  • amino acids
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23
Q

What is absorbed in the ileum? (2)

A
  • B12
  • bile salts
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24
Q

What is produced when dietary fibre is fermented in the colon?

A

short-chain fatty acids

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25
Q

Where does carbohydrate digestion begin?

A

mouth that salivates amylase

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26
Q

what does the acidic pH of the stomach do?

A

destroy salivary amylase

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27
Q

What happens to un-broken down starch?

A

cleaved by pancreatic amylase in pancreatic juice

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28
Q

what do brush-border enzymes do? (2)

A
  • act on resulting a-dextrins
  • clipping off one glucose at a time
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29
Q

what is maltose broken down into? (2)

A
  • glucose + glucose
  • broken down by maltase
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30
Q

what is sucrose broken down into? (2)

A
  • glucose + fructose
  • broken down by sucrase
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31
Q

what is lactose broken down into? (2)

A
  • glucose + galactose
  • lactase
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32
Q

How is carbohydrate absorbed? (4)

A
  • monosaccharides pass from the lumen of the small intestine through the apical membrane
  • via facilitated diffusion (fructose) or active transport coupled with Na+ (glucose + galactose)
  • move out through basolateral surfaces via facilitated diffusion
  • enter capillaries
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33
Q

How is protein absorbed? (3)

A
  • begins in the stomach with pepsin
  • enzymes in pancreatic juice (trypsin, chymotrypsin, carboxypeptidase, elastase) continue to break down proteins into peptides
  • protein digestion is completed by two peptidases in the brush border
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34
Q

What does amino peptidase cleave off to?

A

amino acids

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35
Q

What does dipeptidase split?

A

dipeptides to single amino acids

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36
Q

where are amino acids absorbed? (2)

A
  • duodenum
  • jejunum
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37
Q

where do the amino acids enter and how? (2)

A
  • capillaries
  • via diffusion
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38
Q

How are lipids digested? (6)

A
  • emulsification of lipid by adding bile salts
  • digestion by lipase
  • free fatty acids + bile salts forming micelles
  • micelles cross the epithelium
  • triglyceride + protein forming chylomicron
  • chylomicron enters secretory vesicle
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39
Q

what do micelles transport?

A

soluble monoglycerides

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40
Q

where do micelles transport monoglycerides and why? (2)

A
  • surface of enterocyte
  • to be absorbed
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41
Q

What happens to fats inside the enterocyte (epithelial cell) (5)

A
  • monoglycerides are resynthesised into TAG
  • TAG is packaged with cholesterol + fat soluble vitamins in chylomicrons
  • chylomicrons are released by excytosis in secretory vesicles at the basolateral surface of the enterocyte
  • they enter lacteals (lymphatic vessels)
  • chylomicrons cant enter capillaries as they are too large
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42
Q

What does the myenteric plexus stimulate? (3)

A
  • muscles to contract in peristaltic waves
  • promotes secretion of intestinal juices
  • allows sphincter to open
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43
Q

what are cells of the liver called?

A

hepatocytes

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44
Q

what does the liver secrete?

A

bile

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45
Q

what does bile consist of? (6)

A
  • water
  • bile salts (form micelles)
  • cholesterol
  • lecithin
  • bile pigments (main one is bilirubin)
  • several ions
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46
Q

what do lipids combine with to form chylomicrons?

A

proteins

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47
Q

what do lipids and proteins combine to form?

A

chylomicrons

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48
Q

where do chylomicrons travel?

A

in the blood

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49
Q

what is removed in the blood by hepatocytes?

A

remnants of chylomicron

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50
Q

what does vLDL stand for?

A

very low density proteins

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51
Q

where do vLDLs form?

A

in hepatocytes

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52
Q

what is the role of vLDLs?

A

transport triglycerides synthesised in hepatocytes to adipocytes for storage

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53
Q

How are vLDLs converted to LDLs? (2)

A
  • Apo C-2 activates endothelial lipoprotein lipase which removes fatty acids
  • vLDLs are converted to LDLs
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54
Q

What % of cholesterol do LDLs carry?

A

75%

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55
Q

where do LDL deliver cholesterol? (2)

A

to cells throughout the body for…
- preparing cell membranes
- synthesising steroid hormones and bile salts

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56
Q

what happens if LDLs are present in excessive numbers? (3)

A
  • deposit cholesterol in and around smooth muscle fibres in arteries
  • forming fatty plaques
  • increasing risk of CVD
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57
Q

what is the role of HDLs? (3)

A
  • to remove cholesterol from body cells and blood
  • transport it to the liver for elimination
  • prevent accumulation of cholesterol in the blood
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58
Q

what does the body need cholesterol for?(6)

A
  • myelin sheath
  • plasma membrane
  • intracellular transport
  • cell signalling
  • bile
  • precursor for vitamin D and steroid hormones
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59
Q

sources of cholesterol

A
  • food
  • synthesised by hepatocytes (most)
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60
Q

What happens in cholesterol metabolism? (4)

A
  • oxidised by the liver into a variety of bile acids
  • 95% of bile acids reabsorbed from intestines, remainder lost in faeces
  • in the colon, cholesterol can be metabolised by the colonic bacteria
  • converted to coprostanol and excreted in the faeces
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61
Q

Name 5 things that control parietal cell acid (HCl) output

A
  • histamine - stimulating
  • gastrin - stimulating
  • Ach - stimulating
  • prostaglandins (E2 and I2) inhibiting
  • somatostatin - inhibiting
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62
Q

How is the gut secretion stimulated? (4)

A
  • gastrin released from G cells
  • gastrin acts on CCK2 receptors on ECL cells to release histamine
  • histamine acts on parietal cells H2 receptors to elevate CAMP that activates the secretion of acid by the proton pump
  • direct vagal stimulation also provokes acid secretion and releases Ach that acts on parietal cells M3 receptors
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63
Q

How is gut secretion inhibited?

A

somatostatin excrete a tonic/inhibitory influence on G cells, ECL cells and parietal cells

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64
Q

What is the mechanism of proton pump inhibitors? (3)

A
  • irreversibly blocks the H+K+ATPase of parietal cells
  • reduces gastric acid secretion by up to 99%
  • aids the healing of duodenal ulcers, reduces pain from indigestion
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65
Q

What is the mechanism of histamine H2 receptor antagonists? (2)

A
  • competitively inhibit histamine actions at H2 receptors in upper GI tract
  • inhibits gastric acid secretion
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66
Q

what is the role of antacids?

A
  • directly neutralise acid
  • mainly salts of magnesium and aluminium are used
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67
Q

What type of epithelium is the stomach?

A

simple columnar epithelium

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68
Q

what type of epithelium is the mouth, pharynx and oesophagus?

A

stratified squamous epithelium

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69
Q

what three structures are made up of stratified squamous epithelium?

A
  • mouth
  • pharynx
  • oesophagus
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70
Q

What are the arteries that branch of the coeliac trunk? (5)

A
  • left gastric
  • right gastric
  • left gastroepiploic
  • right gastroepiploic
  • short gastric artery
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71
Q

which nerve supplies the stomach?

A

vagus

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71
Q

what does the vagus nerve control? (2)

A
  • secretomotor
  • peristaltic movements
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72
Q

what does the sympathetic nerves control? (2)

A
  • visceral
  • vasculature
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73
Q

how long is the duodenum?

A

25cm

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74
Q

what are the 4 parts of the duodenum?

A
  • superior
  • descending
  • horizontal
  • ascending
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75
Q

describe the superior duodenum (2)

A
  • peritoneal
  • contains CBD
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76
Q

describe the descending duodenum (2)

A
  • retroperiotneal
  • receives CBD via hepatopancreatic ampulla (of Vater) at the major duodenal papilla
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77
Q

describe the ascending duodenum (2)

A
  • duodenojejunal flexure
  • ligament of treats
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78
Q

describe the horizontal duodenum (2)

A
  • retroperitoneal
  • IVC and aorta are posterior
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79
Q

What is pharmacodynamics?

A

how a drug works on the body

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80
Q

What is pharmacokinetics?

A

decided route of administration of a drug

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81
Q

What does ADME stand for?

A
  • A - absorption
  • D - distribution
  • M - metabolism
  • E - excretion
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82
Q

How are drugs absorbed? (4)

A
  • diffusion
  • carrier mediated (protein assisted)
  • paracellular (between cells)
  • efflux transport
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83
Q

the stronger the acid/base nature of the drug, the…

A

…harder it is to absorb them

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84
Q

what are peptic ulcers caused by? (2)

A
  • bacterial infection
  • disruption of the stomach mucosal lining
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85
Q

how you differentiate between a stomach and a duodenal ulcer?

A
  • stomach ulcer - pain soon after eating a meal
  • duodenal ulcer - pain 2-3 hours after eating
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86
Q

what do parietal cells produce?

A

protons to elevate pH of the stomach

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87
Q

what do neck cells produce?

A

lining for the stomach

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88
Q

what do chief cells produce?

A

pepsinogen

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89
Q

H+ is pumped into the lumen in exchange for what?

A

K+ via proton pump

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90
Q

what pharmacology can be used for acid secretion? (4)

A
  • proton pump inhibitors
  • produgs
  • histamine inhibitors
  • NSAIDS
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91
Q

How do PPIs control acid secretion? (3)

A
  • decrease H+ secretion by parietal cells
  • increases pH
  • allows stomach to heal lining
92
Q

What is used for the eradication of H.Pylori?

A
  • amoxicillin + clarithromycin
  • amoxicillin + metronidazole
93
Q

how do histamine inhibitors control acid secretion? (5)

A
  • H2 receptors elevates action of adenencyclase
  • produces cAMP
  • activates protein kinase A (switches protein on/off)
  • blocks h2 receptors
  • decreases acid production
94
Q

how do NSAIDs control acid secretion? (3)

A
  • irreversible inhibitor
  • blocks COX enzyme
  • prevent conversion to prostaglandins
  • prostaglandins decrease acid secretion
95
Q

what is the role of prostaglandins? (2)

A
  • decrease acid secretion
  • increase mucus and bicarbonate secretion
96
Q

what are the types of cells in the stomach? (5)

A
  • mucous cells
  • parietal cells
  • chief cells
  • enteroendocrine
  • stem cells
97
Q

what is gastrin released by?

A

stomach

98
Q

what is secretin released by?

A

duodenum

99
Q

what is cholecystokinin released by?

A

duodenum

100
Q

what is somatostatin released by?

A

D-cells

101
Q

what is gastrin released in response to?

A

food

102
Q

what is secretin released in response to?

A

acid

103
Q

what is cholecystokinin released in response to?

A

food

104
Q

what is somatostatin released in response to?

A

acid

105
Q

what does the stomach secrete? (3)

A
  • pepsin
  • gastric acid
  • lipase
106
Q

how does acid secretion work? (7)

A
  • ECC cells release histamine
  • binds to H2 receptor, activates adenylate cyclase to cAMP
  • G cells release gastrin, binds to CCK2 receptors, activates phospholipase C, releases cytosolic calcium Ca++
  • gastrin stimulates parietal cells to release histamine
  • intramural neurons release Ach, binds to M3 receptors, increases intracellular calcium
  • cAMP systems activate downstream protein kinases
  • this activates H+K+ ATPase (proton pump)
107
Q

what is the role of gastric acid in absorption?

A

protein denaturation

108
Q

what is the role of pepsin in absorption?

A
  • protein digestion
109
Q

what is the role of gastric lipase in absorption? (3)

A
  • digestion of triaglycerol
  • absorption of alcohol
  • acidic drugs
110
Q

what is the role of pancreatic amylase in digestion?

A

digestion of starch

111
Q

what is the role of lipase in digestion?

A

digestion of triaglycerol

112
Q

what is the role of phospholipase in digestion?

A

digestion of phospholipids

113
Q

what is the role of trypsin, chymotrypsin and elastase in digestion?

A

digestion of proteins

114
Q

what are zymogens?

A

proteins secreted as inactive precursors that are activated after secretion

115
Q

what are the end products of enzyme digestion? (3)

A
  • carbohydrates broken down into disaccharides (maltose, sucrose, lactose)
  • protein broken down into dipeptides and free amino acids
  • fat broken down into monoglycerides, long chain fatty acids and glycerol
116
Q

what are the end products of macronutrient digestion? (3)

A
  • carbohydrates broken down into glucose, galactose, fructose, lactate
  • protein broken down into amino acids
  • fat broken down into short chain fatty acids and chylomicrons
117
Q

what is dietary fibre? (2)

A
  • remains of plant cell walls that are resistant to digestion
  • recommended 18g/day
118
Q

what is the glycemic index?

A

is the relative ability of carbohydrate food to increase blood glucose levels
- low value <55g is slowly digested = slow release of glucose

119
Q

what are the benefits of dietary fibre? (4)

A
  • increased clearance of cholesterol
  • slower absorption beneficial in diabetes
  • bile acids have tumour-promoting action
  • anti-cancer actions
120
Q

what % of protein is absorbed in the gut?

A

92%

121
Q

what % of fat is absorbed in the gut?

A

95%

122
Q

what % of carbohydrate is absorbed in the gut?

A

99%

123
Q

what % of alcohol is absorbed in the gut?

A

100%

124
Q

what is the main fat in oils/butter?

A

triacylglyceride (TAGs)

125
Q

how much fat do we ingest in a day?

A
  • 100-150g
  • 40% of our diet
126
Q

how many kilocalories is 1g of fat?

A

9 kcal

127
Q

why is emulsification important? (2)

A
  • churning of stomach emulsifies the bulk triacylglycerides into small droplets
  • larger surface area for enzymes to act on
128
Q

what prevents small triacylglycerides from re-aggregating to bigger forms? (3)

A
  • particles coated with bile salts
  • more amphipathic, the polar surface prevents re-aggregating whilst allowing lipase to break it down
  • bile salts digest to micelles for uptake into enterocytes
129
Q

what is the major enzyme of fat digestion?

A

pancreatic lipase

130
Q

what other enzyme anchors bile salt-coated fat droplets?

A

colipase

131
Q

what are the stages of lipid absorption? (5)

A
  • breakdown of products of lipid digestion are coated with bile salts to form micelles
  • micelles travel to apical brush border of intestinal epithelial cells to release products for digestion
  • inside Ecs, lipid products are re-esterified with fatty acids. Produces phospholipids, cholesterol and TAGs
  • these lipids bind to lipo proteins to form chylomicrons
  • chylomicrons migrate to basolateral membrane of ECs
    ready for exocytosis into lacteals and blood
132
Q

what is the most common cause of chronic pancreatitis?

A

alcohol consumption

133
Q

what is the result of chronic pancreatitis? (2)

A
  • produces insufficient amounts of lipase needed for lipid digestion
  • results in excretion of greasy stools
134
Q

what are the % components of bile? (3)

A
  • water - 97%
  • bile salts - 0.7%
  • cholesterol - 0.06%
135
Q

what are bile acids?

A

breakdown products of cholesterol

136
Q

what are colic and chenodeoxycholic acids?

A

primary bile acids made in liver

137
Q

How is cholecystokinin (CCK) released? (3)

A
  • CCK releases from duodenal mucosa when food enters intestine
  • CCK in blood stimulates gallbladder to release bile
  • contraction of gallbladder, relaxation of sphincter of Oddi
138
Q

what are the types of gallstones? (2)

A
  • cholelithiasis - stones in gallbladder
  • choledocholithiasis - stones in ducts of billary tree
139
Q

what happens in the absence of bile salts?

A

fatty acids and 2-MAG are absorbed much more slowly

140
Q

where do chylomicrons enter circulation?

A

thoracic lymph duct

141
Q

what do chylomicrons transport?

A

dietary fat

142
Q

where do chylomicrons transport dietary fat to and from?

A

from intestines to tissues via the plasma

143
Q

what happens to the plasma when chylomicrons enter?

A
  • plasma goes opaque
  • clears again in 1 or 2 hours as they get metabolised
144
Q

which artery supplies the foregut?

A

coeliac trunk

145
Q

which artery supplies the midgut?

A

superior mesenteric

146
Q

which artery supplies the hindgut?

A

inferior mesenteric

147
Q

where does the mesentery stretch to and from?

A

posterior wall to the anterior wall in the forgut only

148
Q

what is the direction and the degree to which the midgut rotates?

A

270 degrees anticlockwise

149
Q

which nerve supplies the posterior wall of the foregut?

A

right vagus

150
Q

which nerve supplies the anterior wall of the foregut?

A

left vagus

151
Q

what fuses together to form the pancreas?

A

ventral and dorsal pancreatic buds

152
Q

which week does the foregut form?

A

end of 5th week

153
Q

which weeks does the pancreas form?

A

weeks 5th to 8th

154
Q

what happens between 6-12weeks?

A

herniation of midgut loop

155
Q

name 3 midgut rotation abnormalities?

A
  • omphalocele
  • umbilical hernia
  • remnants of yolk stalk
156
Q

what is the order of the embryological kidneys? (3)

A
  • pronephros
  • mesonephros (temporary kidneys)
  • metanephros
157
Q

what grows into the cloaca?

A

mesodermal tissue

158
Q

what does the partition in the cloaca form?

A

primital uritogenital sinus

159
Q

what covers the transverse colon?

A

greater omentum

160
Q

what is mesentery made up of?

A

two bits of peritoneum stuck together

161
Q

Wha are the layers of the abdominal cavity? (7)

A
  • skin
  • campers fascia
  • scarpus fascia
  • external oblique
  • internal oblique
  • transverse abodominis
  • rectus abdominis
162
Q

where is the external oblique inserted?

A
  • linea alba
  • inferior 8 ribs
163
Q

where is the internal oblique inserted?

A
  • linea alba
  • ribs 10-12
164
Q

where is the transverse abdominis inserted?

A
  • xiphisternum
  • 9th costal cartilage
165
Q

where is the rectus abdominis inserted?

A
  • crest of pubis
  • 5-9th costal cartilages
166
Q

what makes up the floor of the inguinal canal?

A

inguinal ligament

167
Q

what makes up the anterior wall of the inguinal canal?

A

aponeurosis of external oblique

168
Q

what makes up the roof of the inguinal canal?

A

internal oblique

169
Q

what makes up the posterior of the inguinal canal?

A

transversalis fascia

170
Q

what are the functions of the anterolateral abdominal wall? (4)

A
  • moves trunk
  • supports intestines
  • depresses ribs
  • increases intra-abdominal pressure
171
Q

what is the omentum?

A

folds of peritoneum connecting stomach with other organs

172
Q

what does the lesser omentum connect?

A

stomach to liver

173
Q

which nerve supplies small intestine?

A

vagus

174
Q

which artery supplies small intestine?

A

superior mesenteric

175
Q

what epithelium makes up the small intestine?

A

simple columnar epithelium

176
Q

what is the role of the small intestine?

A

absorption of nutrients

177
Q

what are the features of the jejunum? (4)

A
  • thicker wall
  • proximal 2/5 of SI
  • long vasa recta
  • main site of nutrient and water absorption from chyme
178
Q

what are the features of the ileum? (4)

A
  • thinner wall
  • short vasa recta
  • increase arcades, more fat
  • distal 3/5 of SI
179
Q

what is Meckels diverticulum? (3)

A
  • slight bulge in the SI present at birth
  • remnant of vitelline
  • 2% of population, 2 inches in length
180
Q

what are the features of the large intestine? (5)

A
  • 5ft long
  • 2 flexures - hepatic and splenic flexures
  • taniae coli - contract to move faecal matter along intestines
  • haustra - ‘buldges’
  • epiploicae - ‘fat deposits’
181
Q

how to tell the difference between the large intestine and rectum? (2)

A

Rectum has
- no haustra
- no epiploicae

182
Q

what epithelium makes up the anal canal above the pectinate line?

A

columnar epithelium

183
Q

what epithelium makes up the anal canal below the pectinate line?

A

stratified squamous

184
Q

what epithelium makes up the anal canal below the anocutaenous line?

A

keritised stratified squamous

185
Q

which nerves supply the smooth muscle of the anal canal?

A

parasympathetic nerves S2, S3 and S4

186
Q

what role do visceral sensory fibres have in the rectum?

A

sense faecal matter and triggers parasympathetic nerves

187
Q

what are the stages of defecation? (5)

A
  • faeces stretch rectum and stimulate stretch receptors that transmit signal to the spinal cord
  • spinal reflex stimulates rectum contraction
  • relaxes internal anal sphincter
  • impulses from brain prevent untimely defecation by keeping external anal sphincter contracted
  • defecation only occurs when sphincters relax
188
Q

what is the function of the pancreas?

A
  • endocrine - blood sugar control
  • exocrine - secretion of digestive enzymes
189
Q

what two structures join together at the duodenum?

A
  • common bile duct
  • pancreatic duct
190
Q

where do the CBD and pancreatic duct join together?

A
  • hepatopancreatic ampulla
191
Q

which two structures join together to form the common hepatic?

A
  • right and left hepatic ducts
192
Q

what joins the common hepatic duct to become the CBD?

A

cystic duct

193
Q

what is the function of the spleen? (2)

A
  • RBCs
  • immune system
194
Q

where is the spleen found?

A

at ribs 9-11

195
Q

what is the function of the kidney?

A
  • homeostasis
  • removal of excess organic molecules from the blood
196
Q

where does the kidney receive blood? (2)

A
  • renal arteries
  • drains into renal veins
197
Q

what is the ligamentum teres?

A

remnants of the umbilical vein

198
Q

what is the ligamentum venousum?

A

remnants of ductus venous

199
Q

what is the porta hepatis made up of? (3)

A
  • portal vein
  • hepatic artery proper
  • bile duct
200
Q

what % of oxygen does the liver use?

A

20-30%

201
Q

what is the role of the portal vein?

A
  • carries blood (low O2) from the small to large intestine to liver
  • high in nutrients
202
Q

what is the role of the hepatic artery? (2)

A
  • from abdominal aorta
  • carries oxygenated blood from heart to liver
203
Q

what is the role of the bile duct?

A
  • carries bile from liver/gall bladder to the duodenum
204
Q

what is the liver made up of?

A
  • liver lobules (50,000-100,000)
205
Q

what happens in the liver lobules? (3)

A
  • blood from hepatic artery and portal vein mix together in sinuses then drain into central vein
  • sinuses surrounded by endothelial cells have large pores allowing large macronutrients through (proteins, fats)
  • other molecules are processed by hepatocytes
206
Q

what % of the liver is made up of hepatocytes?

A

80%, 300 billion

207
Q

what are the functions of the liver? (5)

A
  • phagocytosis
  • bile salts
  • storage
  • detoxification
  • synthesis
208
Q

what is the purpose of metabolism in the liver?

A

maintenance of plasma levels of metabolites and energy substrates (energy homeostasis)

209
Q

what is glucogeneosis?

A
  • production of glucose from other compounds
210
Q

what is the purpose of carbohydrate metabolism? (3)

A
  • maintains blood glucose at 5.5nM
  • takes up blood glucose from plasma
  • majority is converted to glucose 6 phosphate, some to fatty acids and a small amount for ATP synthesis
211
Q

secretion of glucose is trigged by? (2)

A
  • derived from liver glycogen
  • gluconeogenesis from lactate, glycerol or amino acids
212
Q

secretion of glucose is promoted by? (3)

A
  • cortisol
  • glucagon
  • epinephrine
213
Q

what happens in the Cori cycle? (2)

A
  • transports lactate generated in muscle to the liver
  • converts back to glucose via gluconeogenesis
214
Q

what happens in the alanine cycle? (3)

A
  • degradation of proteins
  • amino acids transferred to pyruvate, giving rise to alanine
  • transported to liver, converted to glucose, nitrogen to urea
215
Q

what are three things to occur in lipid metabolism?

A
  • synthesises TAGs, phospholipids and fatty acids from acetate
  • uptake of plasma acids
  • cholesterol synthesis
216
Q

what happens during cholesterol synthesis?

A
  • forms acetate units
  • lipoprotein complexes for transport in blood
  • excess lipoproteins converted to bile acids or excreted within bile
217
Q

what happens during the uptake of plasma acids?

A

conversion of ketone bodies for energy or excretion

218
Q

what happens during amino acid metabolism?

A
  • liver breaks down excess amino acids which release nitrogen
  • converted to urea for excretion
  • carbon skeleton enters metabolism through gluconeogensis and Krebs cycle
  • products ammonia (toxic)
219
Q

what do bile salts conjugate with? (2)

A
  • glycine
  • taurine
220
Q

what are the functions of bile salts? (5)

A
  • increase non-polar compound solubility
  • amphipathic
  • detergent/emulsifer
  • forms lipids into droplets for digestion (lipase)
  • forms micelles
221
Q

what is the main cause of jaudice?

A

bilirubin accumulation in the blood

222
Q

what are the 3 major causes of jaundice?

A
  • pre-hepatic
  • hepatic
  • post hepatic
223
Q

what is the cause of pre-hepatic jaundice?

A

excess haemolytic, unconjugated bilirubin build up

224
Q

what is the cause of hepatic jaundice?

A

impaired hepatocyte function reduces bilirubin

225
Q

what is the cause of post-hepatic jaundice? (2)

A

-bile drainage obstructed
-build up of conjugated bilirubin

226
Q

what are the stages of liver damage? (4)

A
  • healthy liver
  • fatty liver
  • fibrosis
  • cirrhosis
227
Q
A

ALS (10 decks)

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